Background: The reactivity of cerebral arteries to different stimuli varies according to vessel size, Whether nitric oxide mediates hypoxic vasodilation is controversial. The authors considered this question by measuring the diameter of pial arteries and arterioles with or without exposure to the nitric oxide synthase inhibitor, N omega-nitro-L-arginine methyl ester (L-NAME). Methods: The cranial window technique, combined with microscopic video recording, was used in an experiment involving 20 cats anesthetized with fentanyl and midazolam. The diameters of pial arteries and arterioles mere measured under the following conditions: (1) normoxia (Pa-o2 > 100 mmHg); (2) hypoxia (Pa-o2 < 45 mmHg); (3) normoxia with L-NAME infusion; and (4) hypoxia with L-NAME infusion. Changes in vessel diameter mere analyzed with respect to artery size. Results: Under hypoxic conditions, arteries and arterioles smaller than 200 mu m were dilated significantly (P < 0.05). In arterioles smaller than 200 mu m, L-NAME attenuated this hypoxic vasodilation (P < 0.05). In contrast, under normoxic conditions, L-NAME caused significant vasoconstriction in arteries larger than 100 mu m but not in arteries smaller than 100 mu m. Conclusions: Arteries and arterioles smaller than 200 mu m are dilated by hypoxia, and nitric oxide contributes to this process, Nitric oxide synthesis may also be related to the regulation of resting vascular tone in arteries larger than 100 mu m.